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MicroRNA‐1 facilitates hypoxia‐induced injury by targeting NOTCH3
Author(s) -
Xu Jinjin,
Cao Dandan,
Zhang Daping,
Zhang Yuan,
Yue Yuxia
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29663
Subject(s) - autophagy , apoptosis , microbiology and biotechnology , cell growth , hypoxia (environmental) , downregulation and upregulation , microrna , gene knockdown , cell , chemistry , programmed cell death , cancer research , biology , biochemistry , gene , organic chemistry , oxygen
Abstract Cell proliferation, apoptosis, and autophagy have been reported to be related to myocardial ischemia injury. MicroRNAs have attracted wide attention on regulating cell proliferation, apoptosis, and autophagy. miR‐1 expression has been reported to be dysregulated in cardiac tissue or cells with hypoxia, while the exact roles as well as underlying mechanism remain poorly understood. In this study, we investigated the potential roles of miR‐1 in cell proliferation, apoptosis, and autophagy in hypoxia‐treated cardiac injury and explored the underlying mechanism using H9c2 cells. Results showed that hypoxic stimulation inhibited cell proliferation and the expression of miR‐1 but promoted cell apoptosis in H9c2 cells. Moreover, overexpression of miR‐1 promoted cell apoptosis and inhibited cell proliferation and autophagy in H9c2 cells treated with hypoxia, while its knockdown played an opposite effect. In addition, bioinformatics, luciferase reporter, and RNA immunoprecipitation analyses indicated that NOTCH3 was a direct target of miR‐1 and its upregulation reversed the effects of miR‐1 on cell proliferation, apoptosis, and autophagy in hypoxia‐treated H9c2 cells. Taken together, our data suggested that miR‐1 promoted hypoxia‐induced injury by targeting NOTCH3, indicating novel therapeutic targets for treatment of myocardial ischemia injury.